Monitoring Endo crine

Func tion
Vivek Moitra, MD, Robert N. Sladen, MB, ChB, MRCP, FRCP, FCCM*

KEYWORDS
 Monitoring  Endocrine  Diabetes  Thyroid disease
 Adrenal disease  Pheochromocytoma  Carcinoid

DIABETES MELLITUS

Diabetes mellitus is a systemic disorder characterized by absolute or relative lack of

insulin, resulting in abnormal carbohydrate metabolism, hyperglycemia, and diffuse
vasculopathy. The underlying comorbidity and consequences of poor perioperative
glycemic control present unique challenges in the monitoring of the surgical patient
with diabetes. Perioperative glycemic control is impeded by multiple factors that affect
blood sugar and pancreatic function, including surgical stress, acute illness, anorexia
and fasting, and the masking of hypoglycemic signs and symptoms by b-blockade
and anesthetics.

Glycosylated Hemoglobin: A Monitor of Long-term Glucose Control

Hemoglobin undergoes continuous nonenzymatic glycation by glucose at the
N-terminal valine residue of the b chain, resulting in a series of glycohemoglobins,
the most prevalent of which is hemoglobin A1c (HbA1c). Cation-exchange chromatog-
raphy can be used to measure HbA1c levels. The concentration of HbA1c provides
a measurement of long-term glycemic control, and may be helpful in the early detec-
tion of diabetes mellitus.
The American Diabetes Association currently recommends a target HbA1c of less
than 7% for patients with type 2 diabetes. Studies support the theory that lower levels
of HbA1c are associated with a reduction in microvascular and neuropathic complica-
tions. In a large retrospective meta-analysis, an increase in HbA1c was associated
with a greater risk of cardiovascular events;1 elevation of HbA1c was associated
with cardiac morbidity and mortality independent of a diagnosis of diabetes. These
results suggest that the risk for coronary heart disease correlates with glucose control
regardless of whether a patient is diabetic.2
In the management of intracranial hypertension, cerebral perfusion pressure may be
decreased by increasing cerebral vascular tone through induced mild hypocapnia. In

Division of Critical Care, Department of Anesthesiology, PH 527-B, College of Physicians and

Surgeons of Columbia University, 630 West 168th St, New York, NY 10032, USA
* Corresponding author.
E-mail address: rs543@columbia.edu (R.N. Sladen).

Anesthesiology Clin 27 (2009) 355–364

doi:10.1016/j.anclin.2009.05.005 anesthesiology.theclinics.com
1932-2275/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
356 Moitra & Sladen

patients with diabetes the vasomotor response to carbon dioxide, as measured by

transcranial Doppler, is impaired, and the degree of impairment correlates with the
levels of HbA1c.3 This finding implies that long-term glucose control may play a role
in the regulation of cerebral vasoreactivity in patients with diabetes. Abnormalities
from autonomic neuropathy of the enteric nervous system are common among
patients with diabetes.4 Short-term hyperglycemia and poor long-term glycemic
control delay gastric emptying,5 resulting in increased gastric fluid volume and risk
of aspiration at anesthetic induction. Routine use of preoperative promotility agents
such as metoclopramide is advocated in practice guidelines for patients with diabetes
to reduce pulmonary aspiration.6 However, a recently conducted prospective trial
demonstrated that after 8 hours of fasting, gastric fluid volumes are small and clinically
inconsequential in patients with type 1 and type 2 diabetes. The investigators
concluded that prokinetic therapy may be essential only for patients with poorly
controlled diabetes and HbA1c values greater than 9%.7
When glycemic control is poor, serum and tissue proteins are glycosylated, and
abnormal collagen is deposited in connective tissues and joints. Patients with diabetes
with a history of chronic hyperglycemia may consequently develop stiff joint
syndrome, resulting in impaired joint mobility. When the cervical and atlanto-occipital
joints are involved, airway exposure and laryngoscopy may become difficult. The risk
of limited joint mobility increases as HbA1c values increase, but there are currently no
data to show that poor glycemic control is predictive of difficult airway management.8

Hyperglycemia: A Monitor of Illness Severity

Observational studies of surgical patients suggest that hyperglycemia is associated
with increased hospital stay, admission to the intensive care unit, postoperative infec-
tions, neurologic events, and the risk of in-hospital mortality.9,10 Patients with newly
diagnosed hyperglycemia, which likely represented undiagnosed diabetes, predia-
betes, or stress-induced hyperglycemia, had a higher in-hospital mortality than
patients with known diabetes and hyperglycemia. Blood glucose values were not
statistically different in both groups.10
Hyperglycemia has emerged as an outcome marker in diverse settings. Several
studies have demonstrated a correlation between blood glucose and the development
of congestive heart failure in patients with and without diabetes after a myocardial
infarction.11–13 After ischemic stroke, the presence of hyperglycemia is associated
with reduced functional capacity, decreased penumbral salvage, and increased final
infarction size.14,15 Trauma patients without diabetes who have hyperglycemia on
admission have a greater risk for longer hospital stay, and increased infection rate
and mortality.16 Although an elevated blood glucose level often reflects the severity
of illness and the stress response, it may itself contribute to organ injury and should
be regarded as a reversible, treatable, and independent determinant of outcome.

Perioperative Glycemic Monitoring

There is considerable evidence that poor intraoperative glucose control may increase
postoperative morbidity and exacerbate postoperative complications such as wound
infection or sternal dehiscence after cardiac surgery.17,18 However, there is no well-es-
tablished parameter for intraoperative ‘‘normoglycemia.’’ The demonstration that post-
operative tight glucose control (80–110 mg/dL) can dramatically decrease morbidity and
long-term mortality19 has received an enormous amount of attention. However, surgical
stress makes it difficult to maintain intraoperative normoglycemia, even with carefully
controlled anesthesia. This situation is exacerbated during nonphysiologic circulatory
states such as cardiopulmonary bypass (CPB). The secretion of large quantities of
 Monitoring Endocrine Function 357

counterregulatory hormones such as epinephrine, glucagons, and cortisol establishes

a state of relative glucose intolerance and insulin resistance. High doses of insulin
may be required to induce normoglycemia, but soon after surgery the levels of these
hormones rapidly decline and patients may be at increased risk for hypoglycemia.20
Nonetheless, several protocols have been offered for intraoperative glucose
management that predictably and safely achieve strict glucose control.17,18,21,22
These have ranged from simple, cost-effective glucose-insulin protocols to achieve
normoglycemia in low-risk patients with diabetes scheduled for elective surgery22 to
more complex glucose-insulin-potassium regimens that have improved outcome in
cardiac surgery patients.17 The ‘‘glucose clamp’’ (hyperinsulinemic normoglycemic
clamp technique) is an alternative approach to overcome insulin resistance during
CPB, in which the dose of the insulin infusion is fixed, and a dextrose infusion is titrated
to achieve normoglycemia.21
Preoperative hyperglycemia and renal failure may predict difficulty in intraoperative
glucose control. Intraoperative normoglycemia is especially difficult in patients with
diabetes with initial blood glucose values of more than 300 mg/dL, and glucose control
in advance of surgery can facilitate intraoperative management.23 A low insulin infu-
sion rate and frequent glucose monitoring may prevent intraoperative hypoglycemia
in patients with compromised renal function.23

THYROID DISORDERS

Patients with thyroid dysfunction who require urgent or elective surgery represent
a particular challenge to anesthesiologists. An understanding of the physiology and
pathophysiology of the hypothalamic-pituitary axis is a prerequisite for effective moni-
toring of thyroid function. The hypothalamus synthesizes thyrotropin-releasing
hormone (TRH), which regulates thyroid stimulating hormone (TSH) secretion by the
anterior pituitary gland. TSH stimulates the synthesis and secretion of triiodothyronine
(T3) and thyroxine (T4) by the thyroid gland. T3 and T4 provide a negative feedback
loop through their suppression of TRH.

Perioperative Outcomes: The Systemic Effects of Thyroid Dysfunction

Hypothyroidism and hyperthyroidism are associated with increased perioperative
morbidity and mortality.24 In the hyperthyroid patient, cardiac output and heart rate
increase, pulse pressure widens, and systemic vascular resistance decreases.25
Thyrotoxicosis is associated with a high incidence of atrial fibrillation and warrants
vigilant electrocardiac monitoring during the perioperative period.24 Close respiratory
monitoring is essential because oxygen consumption (VO2) and carbon dioxide
production (VCO2) are increased, and may coexist with ventilatory muscle weakness,
decreased lung volume, and dyspnea.26,27 Patients are extremely susceptible to
hypopnea or apnea with sedative or anesthetic agents.
In the hypothyroid patient, heart rate, myocardial contractility, and cardiac output
decrease.28,29 Muscle weakness results in hypoventilation and an impaired response
to hypoxia and hypercapnia.30,31 Successful treatment of overt thyroid dysfunction
has been associated with an improvement in survival. Some studies have suggested
that patients with mild to moderate thyroid disease are not at a greater risk of major
perioperative complications.32,33 However, when thyroid dysfunction is severe,
surgery and stress can precipitate myxedema coma or thyroid storm.29
358 Moitra & Sladen

Monitoring Thyroid Function

Thyroid function assays can be a useful tool to evaluate patients with thyroid disorders
and to identify patients at risk for morbidity. They may be less useful or misleading with
entities such as the ‘‘euthyroid sick syndrome’’; subclinical hyperthyroidism (abnormal
TSH levels with normal levels of free T3 and free T4); alterations in protein binding; and
administration of medications such as dopamine, amiodarone, and glucocorticoids.
Under these conditions, clinical, metabolic, and end organ measures may be helpful
in the assessment of thyroid function.25
Although the prevalence of thyroid disorders remains high, there is little evidence to
support the routine screening of asymptomatic patients without risk factors for thyroid
disease.34 The assessment of a patient’s thyroid function begins with an evaluation of
the hypothalamic pituitary axis. In patients with an intact axis and steady-state physi-
ology, TSH levels can be used to monitor thyroid function. Small changes in thyroid
hormone concentration lead to large inverse changes in TSH concentration. Current
guidelines suggest using sensitive assays that can detect a TSH level of 0.02 mU/L.35
Relying on the TSH alone can be misleading if patients have been treated recently for
thyrotoxicosis or have pituitary disease, nonthyroidal illness, or thyroid hormone resis-
tance.36 Total T3 and T4 assays measure free (biologically active) and protein-bound
(biologically inactive) hormone concentrations. Numerous drugs and systemic patholo-
gies affect the degree of protein binding, and measurement of total thyroid hormone
concentrations has been largely replaced by measurement of free hormone concentra-
tions (ie, free T3 and T4).

Monitoring Thyroid Function in the Critically Ill or Hospitalized Patient

Evaluation of thyroid function in patients who are hospitalized is difficult and contro-
versial. Current guidelines suggest that thyroid function tests should not be ordered
for seriously ill patients unless there is a strong suspicion of thyroid disease. A TSH
level alone is inadequate to assess thyroid function in the critically ill patient. Critical
illness is associated with biphasic alterations in the thyroid axis irrespective of a history
of thyroid disease.37 During the first phase of stress, peripheral conversion of T4 to T3
is decreased and TSH levels increase. The initial decrease in T3 levels is related to the
severity of illness.38 During the prolonged phase of critical illness, hypothalamic stim-
ulation is impaired and T3 and T4 decrease without an increase in TSH; indeed an
increase in TSH in the critically ill patient may indicate recovery from severe illness.39

Treatment of Hypothyroidism and Hyperthyroidism

The primary treatment of hypothyroidism is thyroid hormone replacement therapy. In
primary hypothyroidism, TSH concentrations can be used to monitor this treatment.
Free T4 is an insensitive indicator and may be within the normal range when TSH is
inhibited. However, measurement of free T4 is warranted in secondary hypothyroidism
when TSH release is impaired. The treatments for hyperthyroidism are antithyroid
drugs, radioiodine, or surgery. TSH levels are useful for the diagnosis of hyperthy-
roidism, but not for determining its degree of severity. Therefore, measuring free T3
and T4 is necessary to assess the efficacy of treatment. Once steady state is
achieved, TSH can be used to assess the efficacy of therapy.

PARATHYROID DISORDERS

Parathyroid hormone (PTH) regulates the extracellular calcium concentration through

its actions on the bone, kidney, and intestine; in turn, the extracellular calcium concen-
tration is the major determinant of PTH secretion.40
 Monitoring Endocrine Function 359

Monitoring Hypoparathyroidism
Patients may develop hypoparathyroidism and hypocalcemia after thyroidectomy or
removal of a parathyroid adenoma. Hypoparathyroidism may also result from renal
resistance to parathyroid hormone. Ionized serum and urine calcium should be moni-
tored at regular intervals preoperatively. Severe hypocalcemia may be associated with
prolonged QT interval and a predisposition to ventricular arrhythmias, notable
Torsades des Pointes.40 It may also impair cardiac contractility and vascular tone,
but levels are seldom low enough to interfere with coagulation.

Monitoring Hyperparathyroidism
Primary hyperparathyroidism, a common cause of hypercalcemia, is most often asso-
ciated with parathyroid adenomas. Surgical candidates present with several risk
factors. They are more likely to be taking antihypertensive medications; exhibit
T-wave abnormalities and ST-segment depressions on ECG, and have a history of
congestive heart failure, thromboembolic disease, stroke, or diabetes.41 Hypercal-
cemia enhances digitalis toxicity.40
Preoperative imaging of patients undergoing parathyroid surgery includes ultraso-
nography or sestamibi scanning of the parathyroid glands to facilitate an operative
approach.42 Traditionally, successful parathyroidectomy depended on inspection of
all four parathyroid glands with a complete neck dissection. This procedure increases
the risk of inadvertent recurrent laryngeal nerve damage.43 The use of intraoperative
PTH assays can ensure complete parathyroid extirpation without a complete neck
dissection, thus decreasing patient morbidity and the incidence of persistent postop-
erative hypercalcemia.42,44

PHEOCHROMOCYTOMA

Pheochromocytomas are catecholamine-secreting tumors composed of chromaffin

tissue derived from the embryonic neural crest.45,46 Manipulation of the pheochromo-
cytoma during surgical resection releases boluses of catecholamines that may induce
significant hemodynamic perturbation, morbidity, and even mortality. Persistent
hemodynamic fluctuations are also possible after tumor removal.47 Improvements in
perioperative outcomes and reductions in mortality have been associated with
improvements in preoperative and intraoperative monitoring.46

Preoperative Monitoring
The improvement in perioperative outcomes for patients undergoing pheochromocy-
toma resection has been attributed in part to more effective preoperative a- and b-
adrenergic blockade.48 This facilitates preoperative intravascular volume repletion
and attenuates the catecholamine surges associated with intraoperative tumor manip-
ulation. Preoperative monitoring of cardiac function starts with careful history taking
and physical examination focusing on the presence of a catecholamine-induced
cardiomyopathy. Preoperative a- and b-adrenergic blockade can also improve
cardiac function and reverse catecholamine-induced cardiomyopathy.46,49 Echocar-
diography may be a useful tool for detecting cardiac dysfunction and assessing the
efficacy of a-adrenergic blockade. The preoperative electrocardiogram may show
prolonged Q-Tc intervals and an elevated QRS complex reflecting ventricular hyper-
trophy;50 ST-segment and T-wave changes may suggest ischemia. These abnormal-
ities can resolve in the postoperative period.51 Recommendations have been made for
monitoring the adequacy of preoperative pharmacologic therapy.
360 Moitra & Sladen

The adequacy of preoperative a-adrenergic blockade is established by a blood

pressure consistently less than 160/90 mmHg, orthostatic hypotension, resolution of
ST-segment abnormalities, and infrequent premature ventricular contractions.52
Intraoperative Monitoring
Adverse perioperative events are more likely to occur with large tumors and prolonged
duration of anesthesia, and elevations in urinary vanillylmandelic acid, epinephrine,
norepinephrine, and metanephrine have been implicated. Despite the use of a- and
b-adrenergic blockade, patients who were premedicated continued to manifest signif-
icant intraoperative hemodynamic lability.48 Because catecholamine surges are ex-
pected with laryngoscopy and intubation, an intra-arterial catheter should be placed
before induction of anesthesia and together with a central venous catheter will facili-
tate the titration of rapidly acting vasodilators and vasopressors throughout the oper-
ation. Arrhythmias and hypertension may result from skin incision or during tumor
manipulation. Profound hypotension requiring norepinephrine infusion may occur
because of persistent a-adrenergic blockade, inadequate volume repletion, and low
plasma norepinephrine after tumor removal, in the face of a-receptor downregulation.
Blood glucose levels should be monitored frequently because elevated catecholamine
levels depress insulin release and cause hyperglycemia.46

ADRENAL INSUFFICIENCY

An intact hypothalamic-pituitary-adrenal axis (HPA) responds to the stress of surgery,

trauma, and infection by increasing adrenal output of glucocorticoids. Endogenous
glucocorticoids modulate the effect of catecholamines on vascular tone, and gluco-
corticoid deficiency results in vasodilation and hypotension.
Monitoring Adrenal Insufficiency
Primary adrenal insufficiency is uncommon, and occurs as a consequence of autoim-
mune adrenalitis, tuberculosis, and HIV.53 Electrolyte abnormalities such as hypona-
tremia and hyperkalemia may arise from aldosterone deficiency. Suppression of the
HPA axis and adrenal insufficiency is most commonly iatrogenic in nature, induced
by chronic steroid therapy for conditions such as Crohn disease, chronic obstructive
pulmonary disease, asthma, and rheumatoid arthritis.
However, it has been more recently recognized that acute adrenal insufficiency may
be induced in elderly or debilitated patients with acute sepsis. Provocative testing with
an adrenocorticotropic hormone (ACTH) analogue (cosyntropin) can detect relative or
absolute adrenal insufficiency. In patients who were septic and critically ill, with hypo-
tension unresponsive to fluids, an increase in plasma cortisol of more than 9 mg/dL 30
minutes after cosyntropin stimulation identified those who benefited from supple-
mental corticosteroid therapy.54,55 Wider application of preoperative cosyntropin
testing might be useful in identifying those patients who would most benefit from peri-
operative adrenal support with corticosteroids.

CARCINOID TUMORS

Carcinoid tumors are rare and neuroendocrine in origin, arising from chromaffin cells in
the gastrointestinal (GI) tract, and occasionally in the bronchi or lung. Carcinoid
syndrome results from the release of vasoactive mediators such as serotonin, brady-
kinin, histamine, gastrin, and substance P.56–58 Mediators released from carcinoid
tumors in the GI tract enter the portal venous circulation and are usually metabolized
by the liver before they reach the systemic circulation. Therefore, carcinoid syndrome
 Monitoring Endocrine Function 361

is more likely to be discovered with metastatic GI tumors or primary tumors outside of

the GI tract. Serotoninergic manifestations include hypertension induced by vasocon-
striction, and increased GI motility with associated diarrhea, high gastric output, and
hyperglycemia.56 High serotonin levels have been implicated in the development of
carcinoid heart disease, characterized by endocardial fibrosis of right-sided heart
valves, with tricuspid regurgitation and pulmonic stenosis.56,59 Carcinoid tumors are
associated with multiple endocrine neoplasia type 1, and the presence or absence
of parathyroid, pancreatic, and pituitary disease should be identified preoperatively.

Preoperative Monitoring
Preoperative monitoring of the surgical patient with a carcinoid tumor should focus on
the systemic manifestations and location of the tumor. Measurement of 24-hour
urinary 5-hydroxyindoleacetic acid (5-HIAA) helps to confirm carcinoid syndrome.
Although 5-HIAA levels cannot predict the physiologic response to surgical manipula-
tion of the tumor, in the presence of carcinoid heart disease, elevated 5-HIAA levels
are associated with increased perioperative morbidity and mortality.60 A full panoply
of imaging studies including chest radiography, CT scans, MRI, and radionucleotide
scans may be necessary to properly identify the location of the primary tumor and
metastasis.58 Bronchoscopy is indicated if a bronchial site is suspected.57 An echo-
cardiogram should be performed to evaluate the pulmonary and tricuspid valves.

Intraoperative Monitoring
Intraoperative monitoring should include an invasive arterial line to monitor hemody-
namic changes during carcinoid crises or blood loss from resection of a vascular
tumor. Central venous access is helpful for the rapid titration of vasoactive drugs,
but central venous pressure monitoring must be interpreted in the context of possible
right-sided valvular lesions.56

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